Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

282
Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
282
Ischemic Heart Disease: Overview01:17

Ischemic Heart Disease: Overview

2.6K
Ischemic heart disease occurs when the heart's blood supply dwindles, causing an ominous lack of oxygen and nutrients. This deficiency, stemming from reduced or obstructed blood flow, spells danger, leading to heart muscle damage and dysfunction.
Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and...
2.6K
Cardiomyopathy II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

339
Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...
339

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Mitoquinone Prevents Cardiac Dysfunction by Normalizing Mitochondrial ROS and Calcium Handling in Acute Myocardial Infarction.

Acta physiologica (Oxford, England)·2026
Same author

Mitochondrial protein OPA3 sustains cardiac function by regulating calcium handling in male mice.

Nature communications·2026
Same author

Dynamic visualization of physiological CaMKII activity using sensitive FRET biosensors.

bioRxiv : the preprint server for biology·2026
Same author

Targeting Arrhythmogenic Late Sodium Current by FHF1<sub>A</sub>-Derivative FixR in Heart Failure Cardiomyocytes.

Circulation research·2026
Same author

Empagliflozin restores cardiac function in obese-diabetic HFpEF mice but further alters gene expression.

Basic research in cardiology·2026
Same author

Ablation, percolation, and afterdepolarization.

Biophysical journal·2026

Related Experiment Video

Updated: Dec 24, 2025

A Modified Simple Method for Induction of Myocardial Infarction in Mice
04:29

A Modified Simple Method for Induction of Myocardial Infarction in Mice

Published on: December 3, 2021

4.3K

MCUb Induction Protects the Heart From Postischemic Remodeling.

Jiuzhou Huo1, Shan Lu2, Jennifer Q Kwong3

  • 1From the Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati, OH (J.H., M.J.B., K.M.G., M.A.S., J.D.M.).

Circulation Research
|April 18, 2020
PubMed
Summary

The MCUb subunit is a protective cardiac gene induced by injury. Its expression reduces mitochondrial calcium uptake, preventing cell death and pathological remodeling after heart ischemia-reperfusion injury.

Keywords:
calciumheartinfarctionmitochondriareperfusion injury

More Related Videos

Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in G&#246;ttingen Minipigs and Landrace Pigs
14:35

Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs

Published on: April 17, 2021

8.9K
An Experimental Model of Myocardial Infarction for Studying Cardiac Repair and Remodeling in Knockout Mice
09:29

An Experimental Model of Myocardial Infarction for Studying Cardiac Repair and Remodeling in Knockout Mice

Published on: July 14, 2023

1.1K

Related Experiment Videos

Last Updated: Dec 24, 2025

A Modified Simple Method for Induction of Myocardial Infarction in Mice
04:29

A Modified Simple Method for Induction of Myocardial Infarction in Mice

Published on: December 3, 2021

4.3K
Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in G&#246;ttingen Minipigs and Landrace Pigs
14:35

Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs

Published on: April 17, 2021

8.9K
An Experimental Model of Myocardial Infarction for Studying Cardiac Repair and Remodeling in Knockout Mice
09:29

An Experimental Model of Myocardial Infarction for Studying Cardiac Repair and Remodeling in Knockout Mice

Published on: July 14, 2023

1.1K

Area of Science:

  • Cardiology
  • Mitochondrial Biology
  • Molecular Medicine

Background:

  • Mitochondrial calcium (Ca2+) loading is crucial for cellular energy production but can cause cell death during ischemia-reperfusion (I/R) injury.
  • The mitochondrial Ca2+ uniporter (MCU) complex regulates mitochondrial Ca2+ influx, with the MCUb subunit's role in cardiac I/R injury being unclear.

Purpose of the Study:

  • To investigate the function of the MCUb subunit in regulating mitochondrial Ca2+ dynamics and cardiac response to I/R injury.
  • To determine MCUb's role in acute injury and long-term cardiac adaptation following ischemic events.

Main Methods:

  • Generated cardiomyocyte-specific MCUb overexpressing and MCUb gene-deleted (knockout) mouse models.
  • Assessed mitochondrial Ca2+ uptake, mitochondrial permeability transition pore opening, and cardiac remodeling post-I/R injury.
  • Investigated MCUb expression changes in response to I/R and remote ischemic preconditioning.

Main Results:

  • MCUb protein is induced in the heart after I/R injury.
  • MCUb overexpression inhibited mitochondrial Ca2+ uptake and conferred partial protection against I/R injury.
  • MCUb deletion exacerbated cardiac remodeling and infarct expansion following I/R, with increased mitochondrial Ca2+ uptake.
  • Remote ischemic preconditioning induced MCUb expression, correlating with reduced mitochondrial Ca2+ uptake.

Conclusions:

  • MCUb acts as a protective cardiac gene, induced by ischemic injury.
  • MCUb induction mitigates mitochondrial Ca2+ overload and opening of the mitochondrial permeability transition pore.
  • MCUb plays a critical role in reducing pathological cardiac remodeling and infarct expansion after ischemic injury.